A systematic review to establish the frequency of cyclooxygenase-2 expression in normal breast epithelium, ductal carcinoma in situ, microinvasive carcinoma of the breast and invasive breast cancer

• Published in: British journal of cancer 2011-06, Vol.105 (1), p.13-17
• Main Authors: Glover, J A, Hughes, C M, Cantwell, M M, Murray, L J
• Format: Article
• Language: English
• Subjects: 631/208/199; 631/67/2324; 692/699/67/1347; Anti-inflammatory agents; Antibodies; Antiinflammatory agents; Biological and medical sciences; Biomarkers, Tumor - metabolism; Biomedical and Life Sciences; Biomedicine; Breast - metabolism; Breast - pathology; Breast cancer; Breast Neoplasms - metabolism; Breast Neoplasms - pathology; Cancer; Cancer Research; Carcinogenesis; Carcinoma, Ductal, Breast - metabolism; Carcinoma, Ductal, Breast - pathology; Carcinoma, Intraductal, Noninfiltrating - metabolism; Carcinoma, Intraductal, Noninfiltrating - pathology; Clinical Study; Cyclooxygenase 2 - metabolism; Dentistry; Drug Resistance; Drugs; Epidemiology; Female; Gynecology. Andrology. Obstetrics; Humans; Mammary gland diseases; Medical research; Medical sciences; Meta-Analysis as Topic; Molecular Medicine; Neoplasm Invasiveness; Oncology; Prevention; Reviews; Science; Systematic review; Tumors
• ISSN: 0007-0920; 1532-1827
• DOI: 10.1038/bjc.2011.204

Background: Epidemiological studies have suggested a protective effect of cyclooxygenase (COX)-inhibiting non-steroidal anti-inflammatory drugs in breast cancer risk and disease progression. We performed a systematic review to evaluate the frequency of COX-2 expression in normal breast epithelium, ductal carcinoma in situ of breast (DCIS), DCIS-adjoining invasive breast cancer, microinvasive carcinoma of the breast (MICB) and invasive breast cancer. Methods: Literature searches were carried out on MEDLINE, EMBASE and Web of Science from their commencement until September 2010. Primary studies examining COX-2 expression by immunohistochemistry methodology were included. Meta-analyses were carried out using random effects models for individual study estimates of COX-2 expression and pooled to give an overall estimate. Results: The pooled prevalences (95% confidence intervals) of COX-2 expressions were 53% (44–61) in DCIS studies and 42% (36–49) in the invasive breast cancer studies. There were too few studies involving normal breast epithelium, DCIS-adjoining invasive breast cancer and MICB to conduct meta-analyses. Conclusion: The findings from our meta-analyses have shown similar COX-2 expression in DCIS and invasive breast cancer. This may suggest the involvement of COX-2 in early carcinogenesis. Further studies of COX-2 expression in DCIS are required to investigate the use of COX-2 as a potential drug target for prevention of disease progression in DCIS.